With technical improvements in both the detection and classification of various apo(a) isoforms, we continued to study the possible relationship between apo(a) isoforms and the serum lipoprotein(a) (Lp[a]) concentration. After implementation of a recently developed technique for quantitative determination of Lp(a)-cholesterol (Lp[a]-C) concentration, we investigated associations among apo(a) isoforms, Lp(a) concentration and Lp(a)-C concentration in a variety of human sera. In collaborative clinical studies, we further studied the association between apo(a) isoforms and premature thromboembolic events in patients with systemic lupus erythematosus (SLE). We investigated the relative value of apo(a) isoform detection and the conventional risk assessment of measuring the type and titer of anti-cardiolipin antibodies (ACA). Time to premature thromboembolic events from the diagnosis of SLE (Kaplan-Meier method) was significantly less in the medium vs. non-medium apo(a) isoform subsets (p= 0.007, log-rank test) and in the IgG and/or IgM ACA positive vs. negative subsets (p= 0.014). Backward stepwise proportional hazard regression analysis yielded a model in which age at SLE diagnosis, medium- sized apo(a) isoforms, and IgG and/or IgM ACA positivity all were significant predictors of the time from SLE diagnosis to premature thromboembolic event (all p <0.03). Thus, the genetically determined apo(a) isoforms improved the prediction of premature thromboembolism in patients with SLE. In other collaborative studies, we continued to explore the relationship between various apo(a) isoforms and various parameters of fibrinolysis in patients with extreme changes in their clinical thyroid status (from hyperthyroid through euthyroid to severely hypothyroid).